Until now, the pathogenic mechanisms underlying CMT1A aetiology were studied mainly using PMP22-overexpressing rodent models, such as the C22 and the C3 CMT1A transgenic models and the transgenic CMT1A rat model.22,23 These CMT1A rodent models overexpress different copy number levels of human PMP22, giving rise to an array of disease severities. The gene discussed is PMP22; the disease is Charcot-Marie-Tooth disease type 1A.